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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

BCL2/adenovirus E1B 19kDa interacting protein 3-like

This gene is a member of the BCL2/adenovirus E1B 19 kd-interacting protein (BNIP) family. It interacts with the E1B 19 kDa protein, which protects cells from virally-induced cell death. The encoded protein also interacts with E1B 19 kDa-like sequences of BCL2, another apoptotic protector. This protein counteracts the apoptotic inducer BNIP3 and may play a role in tumor suppression. [provided by RefSeq, Mar 2011] (from NCBI)
Top mentioned proteins: BNIP3, bcl-2, CAN, V1a, PrP
Papers using Nix antibodies
Association of RB/p16-pathway perturbations with DCIS recurrence: dependence on tumor versus tissue microenvironment
Lisanti Michael P. et al., In Cell Cycle, 2010
... #A5441); Cav-1 mAb 2297 (BD Transduction Laboratories, #610406); Beclin1 (Novus Biologicals, #NBP1-00085); BNIP3 (Abcam, #ab10433); BNIP3L (Abcam, #ab8399); Beta-galactosidase (GLB1; Abcam, ...
NBR1 is a new PB1 signalling adapter in Th2 differentiation and allergic airway inflammation in vivo
Into Takeshi et al., In Cellular and Molecular Life Sciences, 2009
... used are: anti-TRIF rabbit polyclonal antibody (Alexis; AL227), anti-BAG3 rabbit polyclonal antibody (Abcam; ab86298), anti-BNIP3L (NIX) rabbit polyclonal antibody (Abcam; ab8399), anti-NDP52 (CALCOCO2) rabbit ...
Papers on Nix
Discovery of signature genes in gastric cancer associated with prognosis.
Ma et al., In Neoplasma, Feb 2016
A total of 17 genes were identified as signature genes, such as DAB2, ALDH2, CD58, CITED2, BNIP3L, SLC43A2, FAU and COL5A1.Many signature genes associated with prognosis of GC were identified in present study, some of which have been implicated in the pathogenesis of GC.
Hemin induces mitophagy in a leukemic erythroblast cell line.
Colombo et al., Mendoza, Argentina. In Biol Cell, Feb 2016
Moreover, we provide evidences that hemin induces mitochondrial membrane depolarization and that mitochondria sequestration by autophagy requires the active form of the NIX protein.
Neuronal HIF-1α and HIF-2α deficiency improves neuronal survival and sensorimotor function in the early acute phase after ischemic stroke.
Kunze et al., Heidelberg, Germany. In J Cereb Blood Flow Metab, Feb 2016
In the early acute stage upon stroke, Hif1a/Hif2a double knockout mice exhibited significantly reduced expression of the anti-survival Bnip3, Bnip3L, and Pmaip1.
Cerebrospinal Fluid from Sporadic Amyotrophic Lateral Sclerosis Patients Induces Mitochondrial and Lysosomal Dysfunction.
Srinivas Bharath et al., Bengaluru, India. In Neurochem Res, Jan 2016
Proteomic analysis and validation by western blot indicated that sALS-CSF induced the over-expression of the pro-apoptotic mitochondrial protein BNIP3L.
Mieap-regulated mitochondrial quality control is frequently inactivated in human colorectal cancer.
Arakawa et al., Tokyo, Japan. In Oncogenesis, Dec 2015
BNIP3 and NIX are critical mediators for the Mieap-regulated mitochondrial quality control.
Mitochondrial autophagy: Origins, significance, and role of BNIP3 and NIX.
Ney, New York City, United States. In Biochim Biophys Acta, Oct 2015
BNIP3 and NIX are related multi-functional outer mitochondrial membrane proteins.
Selective removal of mitochondria via mitophagy: distinct pathways for different mitochondrial stresses.
Chen et al., Beijing, China. In Biochim Biophys Acta, Oct 2015
In mammals, different mitophagy effectors, including the mitophagy receptors NIX, BNIP3 and FUDNC1 and the PINK1/Parkin pathway, have been identified to participate in the selective clearance of mitochondria.
BNIP3- and BNIP3L-Mediated Mitophagy Promotes the Generation of Natural Killer Cell Memory.
Sun et al., New York City, United States. In Immunity, Sep 2015
Furthermore, we demonstrated a temporally regulated role for mitophagy-inducing proteins BCL2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3) and BNIP3-like (BNIP3L) in the generation of robust NK cell memory.
ROS and Autophagy: Interactions and Molecular Regulatory Mechanisms.
Zhang et al., Tianjin, China. In Cell Mol Neurobiol, Jul 2015
The internal regulatory mechanisms of autophagy by ROS can be summarized as transcriptional and post-transcriptional regulation, which includes various molecular signal pathways such as ROS-FOXO3-LC3/BNIP3-autophagy, ROS-NRF2-P62-autophagy, ROS-HIF1-BNIP3/NIX-autophagy, and ROS-TIGAR-autophagy. Autophagy also may regulate ROS levels through several pathways such as chaperone-mediated autophagy pathway, mitophagy pathway, and P62 delivery pathway, which might provide a further theoretical basis for the pathogenesis of the related diseases and still need further research.
SEX DETERMINATION. A male-determining factor in the mosquito Aedes aegypti.
Tu et al., Blacksburg, United States. In Science, Jul 2015
Here, we show that an M-locus gene, Nix, functions as an M factor in A. aegypti.
Hypoxia activation of mitophagy and its role in disease pathogenesis.
Chen et al., Beijing, China. In Antioxid Redox Signal, May 2015
Mitophagy receptors include Atg32 in yeast, as well as NIX/BNIP3L, B-cell lymphoma 2/adenovirus E1B 19-kDa-interacting protein 3 and FUN14 domain containing 1 in mammals.
Autophagy as a regulatory component of erythropoiesis.
An et al., Changsha, China. In Int J Mol Sci, 2014
Here, the modulators of autophagy that regulate erythroid differentiation were summarized, including autophagy-related (Atg) genes, the B-cell lymphoma 2 (Bcl-2) family member Bcl-2/adenovirus E1B 19 kDa interacting protein 3-like (Nix/Binp3L), transcription factors globin transcription factor 1 (GATA1) and forkhead box O3 (FoxO3), intermediary factor KRAB-associated protein1 (KAP1), and other modulators, such as focal adhesion kinase family-interacting protein of 200-kDa (FIP200), Ca2+ and 15-lipoxygenase.
Rheb regulates mitophagy induced by mitochondrial energetic status.
Bénard et al., Bordeaux, France. In Cell Metab, 2013
This mitochondrial localization of Rheb promotes mitophagy through a physical interaction with the mitochondrial autophagic receptor Nix and the autophagosomal protein LC3-II.
Differential expression of BNIP family members of BH3-only proteins during the development and after axotomy in the rat.
Geum et al., Seoul, South Korea. In Mol Cells, 2012
three members of the BNIP family, BNIP1, BNIP3 and BNIP3L, are expressed in the developing brain with distinct brain region specificity
BNIP3 and NIX mediate Mieap-induced accumulation of lysosomal proteins within mitochondria.
Arakawa et al., Tokyo, Japan. In Plos One, 2011
The physical interaction of Mieap, BNIP3 and NIX at the mitochondrial outer membrane may play a critical role in the translocation of lysosomal proteins from the cytoplasm to the mitochondrial matrix.
Mechanisms of mitophagy.
Narendra et al., Bethesda, United States. In Nat Rev Mol Cell Biol, 2011
Mitophagy, the specific autophagic elimination of mitochondria, has been identified in yeast, mediated by autophagy-related 32 (Atg32), and in mammals during red blood cell differentiation, mediated by NIP3-like protein X (NIX; also known as BNIP3L).
Mieap, a p53-inducible protein, controls mitochondrial quality by repairing or eliminating unhealthy mitochondria.
Arakawa et al., Tokyo, Japan. In Plos One, 2010
mitochondrial ROS and NIX are essential factors for Mieap-induced accumulation of lysosome-like organelles within mitochondria
Loss of Nix in Pdx1-deficient mice prevents apoptotic and necrotic β cell death and diabetes.
Polonsky et al., Saint Louis, United States. In J Clin Invest, 2010
These results establish Nix as a critical mediator of beta cell apoptosis and programmed necrosis in Pdx1-deficient diabetes.
Nix is critical to two distinct phases of mitophagy, reactive oxygen species-mediated autophagy induction and Parkin-ubiquitin-p62-mediated mitochondrial priming.
Yin et al., Pittsburgh, United States. In J Biol Chem, 2010
molecular events responsible for the different phases of mitophagy and placed Nix upstream of the events
IGFBP7 is not required for B-RAF-induced melanocyte senescence.
Rizos et al., Sydney, Australia. In Cell, 2010
In contrast to the previous report, we demonstrate that B-RAF signaling does not induce IGFBP7 expression, nor the expression of the IGFBP7 targets, BNIP3L, SMARCB1, or PEA15, in human melanocytes or fibroblasts.
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